Strength in diversity: Understanding the pathways to herpes simplex virus reactivation

Suzich, Jon B.; Cliffe, Anna R.

doi:10.1016/j.virol.2018.07.011

Cited by 95 publications

(80 citation statements)

References 153 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Of note, our PCR assay showed co-detection of HSV-1 in CSF, this finding was however not in keeping with negative findings on brain MRI and EEG as well as the patient's overall clinical improvement in the absence of antiherpetic therapy. Given that the patient was HSV-1 IgG-seropositive, we presume that co-amplification of the HSV-1-associated target gene resulted from bystander reactivation of the virus initiated by adjunctive dexamethasone and/or the sympathetic response to the bacterial infection [14]. Secondary reactivation of Herpesviruses in response to disease stress and local inflammation has been previously inferred in some cases of CNS infections [15,16].…”

Section: Discussionmentioning

confidence: 81%

Neurolisteriosis in a previously asymptomatic patient with serum IgM deficiency: a case report

et al. 2020

View full text Add to dashboard Cite

Background: Listeria monocytogenes is an opportunistic pathogen of the central nervous system commonly associated with impaired cell-mediated immunity. We hereby present a case of adult neurolisteriosis where the only immunological feature persistently present was serum IgM deficiency, suggesting that non-specific humoral immunity may also play a central role in the control of neuroinvasion by Listeria monocytogenes. Case presentation: A 62-year-old male who had never experienced severe infections presented with headache, nuchal rigidity and confusion. Neuroimaging was normal and lumbar puncture revealed pleiocytosis (760 leukocytes/mm 3) and hypoglycorrhachia (34 mg/dL). The patient was treated empirically for bacterial meningitis. Indeed, further analysis of the CSF showed infection by Listeria monocytogenes, which was accompanied by reduced serum IgM levels that persisted well beyond the period of acute bacterial infection. Levels of IgG and IgA isotypes, along with peripheral blood counts of major leukocyte subsets, were at the same time largely preserved. Intriguingly, the absence of membrane-bound IgM on B cells was essentially complete in the acute post-infection period leading to a remarkable recovery after 12 months, suggesting that mechanisms other than defective membrane expression are underlying serum deficiency. Conclusions: As far as we know, this is the first reported case of neurolisteriosis associated with IgM deficiency in an adult individual without a history of severe infections or other underlying conditions. A possible role of circulating IgM against invasive disease caused by Listeria monocytogenes, particularly in the early course of hostpathogen interaction, is discussed.

show abstract

Section: Discussionmentioning

confidence: 81%

Neurolisteriosis in a previously asymptomatic patient with serum IgM deficiency: a case report

et al. 2020

View full text Add to dashboard Cite

show abstract

“…VP16 forms a transactivation complex binding in the cytoplasm host cell factor-1 (HCF-1) (protein that contains a nuclear localization sequence), and in the nucleus the homeodomain protein Octamer binding protein-1 (Oct-1). These proteins form a trimeric complex able to activate the immediate early (IE) gene expression [19]. Successful lytic replication is dependent on the expression of the viral IE genes within all infected cells.…”

Section: Pathogenesismentioning

confidence: 99%

Sunlight and Herpes Virus

Mazzarello¹,

Ferrari²,

Decandia³

et al. 2020

Human Herpesvirus Infection - Biological Features, Transmission, Symptoms, Diagnosis and Treatment

View full text Add to dashboard Cite

The Herpesviridae are a family of viruses widely spread in nature that can infect a wide variety of species. After the primary infection, the human alphaherpesvirinae sub-family remains quiescent in the nerve ganglia from which it can periodically reactivate, causing clinical manifestations. Although spontaneous recurrences are possible, a wide variety of internal and external triggers may lead to transformation of the Herpes Simplex and Varicella-Zoster Viruses from a dormant to a proliferative state. Sunlight is a potent stimulus for the alphaherpesvirinae reactivation. The purpose of this paper is to analyze various features of this correlation and several steps you can take to lower your risk of triggering a herpes outbreak after sun exposure. Learning how to reduce the recurrence is extremely important and it is necessary: to perform a gradual and progressive sun exposure; to know what garments to wear; to know the environmental conditions of exposure; to know each skin phototype; to use a protective product against UVB and UVA with sun protection factor suitable for each phototype and environmental conditions.

show abstract

“…Hence, for reactivation to occur, viral lytic gene expression is induced from promoters that are assembled into heterochromatin and in the absence of viral proteins, such as VP16, which are important for lytic gene expression upon de novo infection. Reactivation is therefore dependent on the host proteins and the activation of cellular signaling pathways 3 . However, the full nature of the stimuli that can act on neurons to trigger reactivation and the mechanisms by which expression of the lytic genes occurs have not been elucidated.…”

Section: Introductionmentioning

confidence: 99%

“…In addition, multiple studies have linked persistent HSV-1 infection to the progression of Alzheimer’s disease 2 . Stimuli in humans that are linked with clinical HSV-1 reactivation include exposure to UV light, psychological stress, fever and changes in hormone levels 3 . How these triggers result in reactivation of latent HSV-1 infection is not fully understood.…”

Section: Introductionmentioning

confidence: 99%

Neuronal hyperexcitability is a DLK-dependent trigger of HSV-1 reactivation that can be induced by IL-1

Cuddy

Schinlever

Dochnal

et al. 2020

Preprint

Self Cite

View full text Add to dashboard Cite

Herpes Simplex Virus (HSV) establishes a latent infection in neurons and periodically reactivates to cause disease. The neuronal stimuli that trigger HSV reactivation have not been fully elucidated. Here we demonstrate that HSV reactivation can be induced by neuronal hyperexcitability. Neuronal stimulation-induced reactivation was dependent on voltage-gated ion and hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, demonstrating that neuronal activity is required for reactivation. Hyperexcitability-induced reactivation was dependent on the neuronal pathway of DLK/JNK activation and progressed via an initial wave of viral gene expression that was independent of histone demethylase activity and linked to histone phosphorylation. IL-1β induces neuronal hyperexcitability and is released under conditions of stress and fever; both known triggers of clinical HSV reactivation. IL-1β induced histone phosphorylation in sympathetic neurons, and importantly HSV reactivation, which was dependent on DLK and neuronal excitability. Thus, HSV co-opts an innate immune pathway resulting from IL-1 stimulation of neurons to induce reactivation.

show abstract

Strength in diversity: Understanding the pathways to herpes simplex virus reactivation

Cited by 95 publications

References 153 publications

Neurolisteriosis in a previously asymptomatic patient with serum IgM deficiency: a case report

Neurolisteriosis in a previously asymptomatic patient with serum IgM deficiency: a case report

Sunlight and Herpes Virus

Neuronal hyperexcitability is a DLK-dependent trigger of HSV-1 reactivation that can be induced by IL-1

Contact Info

Product

Resources

About